British autism expert Professor Simon Baron Cohen of Cambridge University does not agree with the USA’s vaccination advocate and rotavirus vaccine patent holder Dr Paul Offit MD that autism is a genetic condition. Here you can see the evidence shows autism is not “genetic”; that Offit is wrong and that Professor Baron Cohen is only partly right.
We demonstrate here that we can consign over 30 years of unscientific medical, psychiatric and psychological papers to the garbage. This brings a scientific approach to the issue since the erroneous genetic myth was first propounded with the publication of Professor Michael Rutter’s paper Infantile autism: A genetic study of 21 twin pairs. J. Child Psychol. Psychiat. 18, 297-321 (1977).
Professor Baron Cohen says:-
“We know that autism is not 100% genetic in origin, since in the case of identical twins (who share 100% of their genes), there are instances of one twin having autism and the other not having it. In fact, the likelihood of the co-twin also having autism where one of them has it (in monozygotic (MZ) pairs) is about 60%. This means that there must be some non-genetic (i.e., environmental) factors that are part of the cause of autism.“ [SOURCE: Professor Baron Cohen's reply to critics of a mooted abortion test for autism reported in the UK's Guardian Newspaper :- Professor Baron Cohen/Stone Correspondence Re: The Guardian New research brings autism screening closer to reality 12/Jan/09]
In other words, it is the 40% of identical twins where only one develops symptoms of autism which tells us autism is not “genetic“. In those cases it must have an environmental [external] cause.
Professor Baron Cohen errs in assuming the 60% of both twins developing autism is evidence autism is ever a genetically “caused” condition. It is not such evidence. The correct medical terminology is whether a condition has an “internal” cause or an “external” one.
Because the twins are genetically identical all we can say for those who both develop autism is their bodies have responded identically to the same set of conditions whether “internal” or “external”. It tells us nothing about whether the cause is internal or external [environmental]. It is neither scientific nor logical to assume the “cause” is internal or external [environmental]. It is wrong to do so and a logical fallacy.
Where both identical twins develop autism, it is more likely than not they have had the same exposure to the same environmental cause. That is more likely than not to happen [60% of the time it seems]. For example, both twins are more likely than not to have their vaccinations at the same time and all other circumstances in their lives at that time are more likely than not to be identical for both.
All human medical conditions whether “internal” or “external” are genetic. Some of us are more susceptible to’ flu than others and some never suffer from it. So it is also logically inappropriate to discuss causes of conditions in terms of being “genetic” because all human conditions are genetic whether the cause is “internal” or “external”. This also demonstrates why it is not wise to rely on medical doctors’ attempts to be scientific. The majority have no formal scientific training or qualifications and frequently make errors of the fundamental kind illustrated here.
We only become ill or develop any condition because we are genetic. Everthing else breaks down. Computers, cars, washing machines and refrigerators breakdown whether for an “internal” cause or an “external” one – they do not and cannot get ‘flu, measles or autism because they are not genetic. If we were not genetic we would not get sick [but we might rust a bit from time-to-time].
There appears to be no scientific evidence autism is any more “genetic” than ‘flu. Feel free to submit a comment if you disagree.
To establish with scientific evidence that any condition has a solely genetic [internal] cause any more than any other illness or disorder requires evidence showing that in some cases there are no possible environmental causes.
The environmental causes have to be eliminated by the collection of evidence in a scientific manner. This has not been done, as the reliance on the twin studies demonstrates.
What we can conclude is that autism is an environmentally [externally] caused condition, with some more susceptible than others, like most other human medical conditions.
What has gone before is non science is because:
- identical twin studies show autism has an environmental [external] cause
- to demonstrate autism has an [internal] ie. solely genetic cause, it is necessary to show autism occurs where no environmental causes apply
- that has never been done
- and that is likely because, as the evidence shows, autism is caused by environmental factors, just like most other human medical conditions
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It should be pointed out that Dr Offit’s views underpin British Government vaccine science, as when Dr David Salisbury wrote to me in 2004:
“Turning to my comments on Newsnight – I suggest you read Paul Offit’s paper – as I have done. On page 126, he states: “Current data suggest that the theoretical capacity determined by diversity of antibody variable gene regions would allow for as many as 109 (1,000,000,000) to 1011(100,000,000,000) different antibody specificities”. And “… then each infant would have the theoretical capacity to respond to about 10,000vaccines at any one time” – not antigens. I was speaking very specifically about the infant immune system’s ability to respond, in the context of the ridiculous suggestion that the new vaccine combination, containing far fewer antigens than the one it will replace, would overload the immune system. My words were “The immune system of a baby has got huge spare capacity to deal with challenge. If we didn’t, the human race wouldn’t survive. But let’s look specifically at vaccine. This has been studied carefully. A baby’s immune system could actually tolerate perfectly well 1,000 vaccines”. At no point did I suggest that 1,000 vaccines would not increase the probability of adverse reactions – a quite different matter.” (Email August 26, 2004 10.03am)
Of course, this is pure nonsense in its own right. It looks like a baby has an official capacity to withstand assault, but the reality may be somewhat different.
We associate Dr Offit less with the practice of science and more with the construction of doctrinaire positions, which at least confuse journalists and their editors.
I am happily amazed that Simon-Baron Cohen actually admitted that autism is not closely tied with genetics.
Perhaps we can move on from here and discover the true causes:
Ergo, we conclude autism is an environmentally [externally] caused condition, with some more susceptible than others, like most other human medical conditions.
Time to check out the universally-given/mandated vaccines, friends,
Aasa
Thank you– I’m thrilled to read someone’s point that, after all, twins do occupy the same environment ! It’s amazing to me that this point is virtually never taken into account, and that everything that happens to them in common is nearly always attributed to genetic cause.
Your headline, “Autism Not Genetic – Says Expert Professor Simon Baron Cohen”, misinforms. Was that deliberate on your part?
SBC clearly says that autism “is not 100% genetic in origin”, and nobody is saying all ASDs are. We know, for instance, that a rubella infection during pregnancy can lead to symptoms of autism. But we also know some ASDs are genetic.
AutismNewsBeat said “But we also know some ASDs are genetic.” on 2009/01/27 at 3:15pm
How? Please cite scientific studies proving some ASDs are “internal” and provide links where available.
Professor Baron Cohen said “We know that autism is not 100% genetic in origin“
The comments here falsely presume that the researchers are simplistic fools. In reality, the twin studies compare DZ twins with MZ twins (and sometimes with non-twin siblings, and also comparing separated from unseparated) and thereby they extract the factors for genetic and environmental. See Folstein & Rutter discussed here: [ Ed note: correct reference here: Folstein S. and Rutter M. Infantile autism: A genetic study of 21 twin pairs. J. Child Psychol. Psychiat. 18, 297-321 (1977)1 PubMed - your reference to blog comments deleted as not acceptable - only peer refereed papers please].
You can also see some elaboration about how the genes would be involved at [ Ed note: your reference to blog comments deleted as not acceptable - only peer refereed papers please].
Reply to robin’s comment made January 27th, 2009 at 3:42 pm
Folstein and Rutter reported 11 pairs of identical (monozygotic, or MZ) twins. Of 11 pairs, 4 (36%) were concordant for strictly diagnosed autism.
Unscientific. That does not prove anything. Environmental causes have not been excluded nor has identical exposure to the same or different environmental causes for the autism in the identical twins.
Next please ……
“A pair of male monozygotic twins concordant for autism is reported.
During pregnancy the mother suffered from severe toxemia, and delivery
occurred 2 months before term. Although there may have been a genetic
influence, it appears that gestational damage was the main etiological
factor for the autism in both children.”
“Early infantile autism in monozygotic twins“. Eshkevari HS. J Autism Dev
Disord. 1979 Mar;9(1):105-9.
There’s a complicating factor here, that makes ASD both environmental and genetic in origin (genetic as in a genetic predisposition to damage). At least some of the genes that have been discovered as being associated with ASD code for glutamate/glutamic acid:
http://www.medpagetoday.com/NeurologyAutism/tb/5082
This peer-reviewed article states: ‘The candidate genes are involved in the trans-synaptic transportation of glutamate, a major excitatory neurotransmitter.” Part of glutamate’s damage is wreaked because it lowers glutathione levels, which is the substance the body makes to remove heavy metals. Glutamate is found in the diet, but it is also found in vaccines (a stabilizer, keeping the live virus alive). So: not only does it increase inflammation in the brain in its own right, in reducing the body’s ability to excrete heavy metals it has a double-whammy effect especially when a vaccine containing it is given at the same time as a vaccine containing mercury/aluminum.
We have been playing with fire too long. It’s time and past for a major review of our medical practices in relation to the ingredients of vaccines.
We need to be careful here [Re: Kibitzer's comment January 28th, 2009 at 2:53 pm]
All human conditions are genetic and much research these days is focussed on finding patentable pharmaceutical treatments and not on finding the causes. Illness and other unwanted conditions may well be avoidable in the first place. But if we do not look for causes, we will never prevent the problems occurring in the first place. The “treatments” may well be unnecessary and it does look like we are causing many more serious problems than we are solving with the current obsession with vaccination at all costs.
I agree with the comment that 60% of identical twins having autism does not prove anything. It certainly does not prove that autism is ‘purely’ genetic in those cases, as both
Twins would have been exposed to same or very similar environmental insults pre- and post-natally. Their bodies would have reacted in similar manners to those insults.
In reply to autismnewsbeat “we also know some ASDs are genetic” – yes, the current estimate is that around 2% of all autism cases are monogenetic in origin. Those cases are extremely important as they have some common underlying molecular mechanisms, which gives us invaluable insights to what could be going wrong, and why, in the other 98%. I have written about those underlying shared mechanisms at some length here http://www.autismcalciumchannelopathy.com
Many environmental insults, including viral infections and environmental toxins, affect those same mechanism that cause autism in those 2% of purely genetic disorder. Unfortunately in order to closely research (and rule out) those environmental insults, we would have to first of all closely scrutinise vaccines.
Apart from toxicological aspects of vaccine injury, we must research possible (auto)immune triggers of various types of vaccine on specific genetic subtypes – one good example are genetic polymorphisms known to be behind vaccine-triggered autoimmune arthritis. This same polymorphism has been found prevalent in autism:
…We report now that the third hypervariable region (HVR-3) of certain DR beta 1 alleles have very strong association with autism. The HVR-3 of DR beta 1* 0401 or the shared HVR-3 alleles DR beta 1* 0404 and DR beta 1* 0404 and DR *0101, was expressed on extended haplotypes in 23 of 50 (46%) autistic subjects as compared to only 6 of 79 (7.5%) normal subjects. …
while:
….The hepatitis B vaccine has been implicated in a few dozen cases of extraarticular, systemic, or inflammatory joint disorders. We report two cases in which hepatitis A vaccination (Havrix, Smith Kline Beecham) was followed by a connective tissue disorder or a spondylarthropathy in two healthy males aged 50 and 24 years, respectively. Both patients were HLA B27-negative but carried the HLA DR1 and/or DR4 antigen. The outcome was favorable after treatment with a corticosteroid or a nonsteroidal antiinflammatory agent. The pathophysiology of immunization-related rheumatic disorders may involve circulating immune complexes and/or a mechanism similar to that seen in reactive arthritis, i.e., a genetically-determined susceptibility to the bacterial or viral antigens contained in vaccines. PMID: 9178394
… Hepatitis B vaccination has been associated with reactive arthritis and rarely rheumatoid arthritis (RA). We defined the clinical, serologic, and immunogenetic background of patients developing RA, soon after recombinant hepatitis B vaccination. METHODS: The clinical, serologic, and HLA antigens of a cluster of firefighters who developed arthritis after prophylactic recombinant hepatitis B vaccination (5 subjects), as well as a second group of sporadic cases of arthritis (6 patients) after hepatitis B vaccination are described. …. CONCLUSION: These polymorphic residues in the binding site of the MHC class II molecules of the affected patients appear capable of binding some peptide sequences of the recombinant vaccine peptides they received and may be responsible for hepatitis B vaccine triggering development of RA in these cases. Recombinant hepatitis B vaccine may trigger the development of RA in MHC class II genetically susceptible individuals. PMID: 9733447
….Logistic regression modelling of DR, treatment, age, time postpartum, and arthropathy revealed that the odds of developing arthropathy was 1.9 times greater (95% CI, 1.07-3.44) after rubella vaccine than placebo. Risk for arthropathy (regardless of rubella vaccination) was also influenced by DR interactions: odds were 8 times greater in individuals with both DR1 and DR4 (95% CI, 1.45-44.02) and 7.1 times greater with both DR4 and DR6 present (95% CI, 1.85-27.52), suggesting that coexpression of these specificities may predispose to postpartum arthropathy. PMID: 9419163
….This study revealed that adult rubella and adult hepatitis B vaccines were statistically associated with chronic arthritis which persisted for at least one year. The etiology for these adverse reactions may involve autoimmune mechanisms. … PMID: 12508767
….A 13-year-old girl developed bilateral chronic anterior uveitis following bacille Calmette-Guérin (BCG) vaccination. HLA testing was negative for B27 but positive for DRB1 *0404, a variant of DR4 often associated with rheumatoid arthritis. The authors propose her HLA repertoire allowed for a BCG-induced abnormal autoimmune response by the mechanism of molecular mimicry… PMID: 18705627
We also must research links between inflammation and oxidative stress-related MIF gene polymorphisms found in autism and susceptibility to serious vaccine reactions:
… There were genetic associations between known functional polymorphisms in the promoter for MIF and autism spectrum disorder-related behaviours. Also, probands with autism spectrum disorder exhibited higher circulating MIF levels than did their unaffected siblings, and plasma MIF concentrations correlated with the severity of multiple autism spectrum disorder symptoms…. PMID: 18676531
On a slightly different note, but no less interesting:
Can unresolved infection precipitate autoimmune disease?
Marks DJ et al Centre for Molecular Medicine, University College London, UK
Autoimmune diseases are frequently postulated to arise as post-infectious phenomena. Here we survey the evidence supporting these theories, with particular emphasis on Crohn’s disease and ankylosing spondylitis. Direct proof that infection establishes persistent autoimmunity remains lacking, although it may provoke a prolonged inflammatory response when occurring on a susceptible immunological background. The argument of infective causality is by no means trivial, since it carries important consequences for the safety of vaccine development. PMID: 16724803
And since autism has long be linked to prenatal viral infections and maternal immune activation, we must research the possibility (and circumstances) of vaccine-reactivation of latent viruses. This mechanism of an induced immune challenge having a trigger-like effect on latent viruses has been suggested to underlie development of CNS autoimmune diseases
…..Based on three cases reported to the Swiss Drug Monitoring Centre SANZ, we postulated previously that vaccinations may trigger reactivation of herpes virus infections due to vaccine-induced immunomodulation. .. PMID: 11103441
In addition, some interesting findings from HIV-related vaccine research that merits looking into (note that, in roughly 40% of infected children, HIV causes neurological symptoms that are completely indistinguishable from ‘common’ autism) : …Although humans are usually exposed to pathogenic viruses, recombinants between a host-adapted vaccine strain and a pathogenic virus might lead to more rapid progression to disease. In addition, the emergence of new variants might be favored…… Therefore, the emergence of more-virulent recombinants of live, attenuated immunodeficiency viruses and less-aggressive wild-type viruses seems to be an additional risk of live, attenuated immunodeficiency virus vaccines…. PMID: 10729127
Thank you for posting about this. Keep up the awesome work!
We have twin boys – now 5 years old (not identical) of which one gradually regressed around 34 months old and dx’d with ASD at 48 months old. I get really tired of people asking why one twin has it and not the other.
Well if the same situation can happen in IDENTICAL TWINS, (one having ASD, the other does not) then it can certainly happen to our fraternal twins!
Recently I came across a news report from out of IOWA under “Autism & Insurance Part 3″ dated Nov 12th 2008. Part of it discussed a family that has IDENTICAL TWIN BOYS of which one has Autism, the other does not. They are having trouble getting the one with ASD covered under insurance. The IDENTICAL TWINS are grandsons to State senator Daryl Beall of Iowa. The news article and video are archived on the news web site and it no longer has the videos. Fortunately, because the reports interested me, I had saved them back in November and recently posted it up for anyone interested:
http://sitekreator.com/CindyRilla/autisminsuranceIA.html
I’ve often wondered what the Beall family thinks why one twin has it and not the other. Maybe at this point, they don’t care but only want proper help and insurance coverage for their one twin son.
[Ed. Visit Cindy's Site and see the videos - Commercial pressure in the US from the insurance industry on Government may well be one way of getting the proper research done into the environmental causes, including vaccines.]
” * identical twin studies show autism has an environmental [external] cause”
Those studies show that the causes are neither entirely environmental nor entirely genetic. If they were entirely environmental, then one would expect that fraternal twins (DZ) would experience the codiagnosis at about the same rate as identical twins (MZ). And they don’t. Not even close.
I think we are finding that a small percentage of cases are entirely genetic (e.g., Fragile X) in that they would lead to autism in any environment, but that most cases involve a combination of genes that establish a vulnerability and environmental factors. There are hundreds of hypotheses about what those environmental factors might be, but little in the way of proof.
Baron-Cohen’s own favorite hypothesis revolves around in-utero exposure to testosterone. From the child’s standpoint, that’s environmental of course. On the other hand, from the mother’s standpoint, it may be genetic.
” * to demonstrate autism has an [internal] ie. solely genetic cause, it is necessary to show autism occurs where no environmental causes apply
* that has never been done”
It has never been done because it can’t be done. How can anyone design a study where a child is exposed to no environmental causes when the full set of environmental factors that can contribute to autism is not known. We’re not even close to knowing what that set is.
I don’t think this genetics-vs-environment argument has been very helpful. It sometimes sounds like both sides are saying that the other is barking up the wrong tree, wasting research resources. But clearly, both genetics and environment are important factors, and both need research. In fact, research into one can aid research into the other. If we find evidence for a particular environmental factor, we can look for genes that may interact with it. If we find a gene that is more common in autistic people, examining the function of that gene may lead us to an environmental trigger.
The glutamate transport gene research cited in the comment above is an example of the latter. It doesn’t prove that dietary glutamate or glutamate in vaccines are triggers that cause autism in some children who have this polymorphism. But it helps direct research attention toward that possibility.
Genetic huh? Here’s genetics for ya, nobody, get that nobody in my family has any history of any form of neurological disorders, yet my son has Aspergers, a higher functioning form of autism.
Explain the genetics in that will ya.